Postgraduate Medicine

ISSN: 0032-5481 (Print) 1941-9260 (Online) Journal homepage: http://www.tandfonline.com/loi/ipgm20

An update on common skin diseases Larry E. Millikan MD & Joseph P. Shrum MD To cite this article: Larry E. Millikan MD & Joseph P. Shrum MD (1992) An update on common skin diseases, Postgraduate Medicine, 91:6, 96-115, DOI: 10.1080/00325481.1992.11701318 To link to this article: http://dx.doi.org/10.1080/00325481.1992.11701318

Published online: 17 May 2016.

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First of three articles on skin diseases

An update on common skin diseases Acne, psoriasis, contact dermatitis, and warts

Preview Numerous therapies are available to control common skin diseases, from the mildest lesion to severe, recalcitrant forms. How should initial treatment be handled? What topical and systemic agents are available for recurrent and refractory cases? Which lesions have the potential for scarring and malignancy? The answers to these questions can guide primary care physicians in selecting optimum therapy to avoid a disfiguring result.

Larry E. Millikan, MD Joseph P. Shrum, MD

tact dermatitis, common warts, and venereal warts.

•!• Many common skin diseases seen by primary care physicians have the potential for recurrence and a refractory course. Failure to resolve the problem may affect a patient's general health and psychological well-being. Fortunately, a wide variety of therapies are available. This article discusses the presenting features and therapeutic options for five common skin diseases: acne, psoriasis, con-

Acne Acne vulgaris is the most common skin disease of adolescents, affecting up to 90% of teenagers. However, acne may affect any age-group, from the newborn to the elderly. PRFSEN'L\TION-Acne has a predilection for skin with high concentrations of sebaceous glands; thus, the face, chest, and back are common sites of in-

volvement. Clinical manifestations vary from mild comedomal disease to pustular and cystic lesions that result in scarring. The three main causes of acne are ( 1) enlargement of the sebaceous glands and increased production of sebum as a result of androgenic stimulation, (2) increased adherence of cells lining the sebaceous follicle, and (3) bacterial colonization on the skin, especially by Propionibacterium

acnes. The pathognomonic lesion of acne is the comedone. Very mild acne may be characterized by just a few closed comedones (whiteheads) or open comedones (blackheads). As acne becomes more severe, other lesions, such as papules, pustules, and cysts, appear. Scarring may develop as a consequence of deep inflammation of a pustule or cyst or excoriation by the patient. The type of lesion found on physical examination determines the degree of severity of acne and its subsequent treatment. 1HERAPY-Comedomal and papular forms of acne usually respond to topical therapy, whereas pustular or cystic acne generally requires systemic therapy as well. TOPICAL AGENTS-The topical medications most frequently used

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Illustration:© 1992. Bret Meredith

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A sudden increase in the severity of acne during antibiotic therapy may reflect underlying gram-negative folliculitis.

for the milder forms of acne are tretinoin (Retin-A), benwyl peroxide, and topical antibiotics. All are available in a variety of vehicles, including lotions, creams, gels, and liquids. The patient's skin type, whether oily or dry, and the patient's personal preference determines which vehicle is best. In general, the greater the percentage of alcohol in a preparation, the more drying it is. Creams and lotions usually are less drying than gels and liquids. A good rule of thumb is to start with the lowest-strength and presumably least-irritating preparation and increase the strength if the patient's response is not satisfactory. Tretinoin is often prescribed for initial treatment of acne. This synthetic vitamin A works primarily by decreasing the cohesiveness of the cells lining the sebaceous follicle, an action that makes it an excellent comedolytic agent. Proper patient instruction regarding its application is essential to reduce the potential for its primary side effect, irritation. Tretinoin should be applied 30 minutes after washing to ensure that the skin is dry. Application on hydrated skin promotes penetration and subsequent irritation. Tretinoin should be applied only once a day, usually at

bedtime. Since it may increase susceptibility to sunburn, use of a sunscreen should be encouraged. Benwyl peroxide, primarily an antibacterial agent, may be applied once or twice a day, generally in the morning and afternoon or evening. It may be used alone or in combination with other topical medications, depending on the severity of the acne. Initiation of treatment with a 2o/o concentration minimizes the primary side effect of irritation. The topical antibiotics most often prescribed for acne are erythromycin and dindamycin. These agents, which primarily reduce the number of bacteria on the skin, also have antiinflammatory effects. Applied once or twice a day, topical antibiotics are useful alone or in combination with other topical antibiotics or with systemic antibiotics. SYSTEMIC AGENTs-Systemic antibiotics are used alone or in combination with topical medications for pustular or cystic acne. Systemic antibiotics reduce the number of resident flora, inhibit activity ofbacteriallipases, and suppress chemotaxis. Tetracycline, the most commonly prescribed oral antibiotic, is usually

given in a dosage of 500 mg twice a day. Alternatives include erythromycin, 500 mg twice a day; minocydine (Minocin), 50 to 100 mg two or four times a day; and double-strength trimethoprim-sulfamethoxawle twice a day. Exact dosages may vary with the extent of disease and the patient's body weight. Treatment can be tapered after acne dears or continued indefinitely if the patient has repeated flares after total withdrawal of treatment. A sudden increase in the severity of acne during antibiotic therapy may reflect underlying gram-negative folliculitis. The resultant pustules and cysts usually respond to ampicillin, 500 mg twice a day. This should be continued until clearing is significant, usually a week or two. Tender papules or cysts of recent appearance may be treated with an intralesional corticosteroid. Injection of triamcinolone acetonide (Aristocort lntralesional or Forte, Cenocort Forte), 1 to 5 mg/ mL, directly into a lesion until slight blanching or an increase in size is noted often dears these lesions in 1 or 2 days. Fat atrophy may occur if the concentration of the intralesional corticosteroid is too high or the volume too large.

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Some different uses of old medications, as well as a few new drugs, have advanced the treatment of acne.

For severe, disfiguring acne that is recalcitrant to standard therapy, isotretinoin (Accutane) is an excellent choice. Its primary mode of action involves reduction of sebum production. However, major fetal defects have occurred in pregnant women taking this teratogen. Abnormalities of the central nervous system, skull, eyes, and other systems have been well documented. Consequently, it is imperative to follow the precautions listed in the package insert with regard to informed consent, pregnancy testing, and birth control measures. In appropriate patients, isotretinoin, 0.5 to 2.0 mg/kg in divided doses for 4 to 5 months, dears the lesions. Most patients require just one course of treatment. Isotretinoin is expensive, relapses do occur in some patients, and in addition to the fetal abnormalities just mentioned, dryness of the skin and mucous membranes, vertebral hyperostoses, and elevation of liver enzyme levels may occur. Nevertheless, some patients with cystic acne are eager to undergo such treatment. While taking isotretinoin, patients should stop using over-the-counter astringents and facial scrubs because they may cause irritation.

Larry E. Millikan, MD Joseph P. Shrum, MD Or Millikan (left), coordinator of this symposium, is professor and chairman and Or Shrum (right) is assistant professor, department of dermatology, Tulane University School of Medicine, New Orleans.

NEW THERAPIES-Some different uses of old medications, as well as a few new drugs, have advanced the treatment of acne. Spironolactone (Aldactone), an antagonist of aldosterone, has antiandrogenic effects. Used in oral doses up to 200 mg daily, it decreases sebum production and results in significant improve-

ment in acne. Azelaic acid is a naturally occurring dicarboxylic acid with antimicrobial actions. When applied topically three or four times a day, it is as effective as benzoyl peroxide, tretinoin, or oral tetracycline. 1 The newest topical medication for acne is an erythromycin-zinc formulation (Theramycin Z).

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As a rule, the thicker the psoriatic plaque, the higher the potency of corticosteroid needed.

Through increased absorption and direct antimicrobial mechanisms, this formulation, used twice daily, has proved comparable to or better than topical clindarnycin in improving acne. 2 lsotretinoin gel has recently been shown to significantly reduce the number of both noninflamed and inflamed lesions in patients with mild to moderate facial acne. 3

Psoriasis Psoriasis affects about 1% of the US population. It can present in a variety of ways and can have disfiguring consequences. PRFSENTATION-Psoriatic lesions may be small and localized or diffuse and inflammatory. At an extreme, psoriasis can result in exfoliative erythroderma. Regardless of the extent of involvement, psoriasis is almost always a cyclic process with relapses and remtsswns. 1HERAPY-Selection of appropriate therapy depends largely on the extent of involvement. Other determining factors include the impact of the disease on the patient's physical and psychological health and the accessibility of therapy. TOPICAL AGENTs-Topical corticosteroids are the medications most often used in the

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United States to treat localized psoriasis. In general, the thicker the plaque, the higher the potency of corticosteroid needed. Physicians should be aware of potential side effects of topical corticosteroids, which include local hypertrichosis, hypopigmentation, and striae. An occlusive dressing can be used alone to flatten out some psoriatic lesions; when used in combination with a topical corticosteroid, it can potentiate the effect of the drug. Crude coal tar and its derivatives have long been used effectively to reduce the thickness and the erythema of psoriatic plaques. The action of coal tar compounds is potentiated when they are combined with UV light in the B range (UVB). Anthralin-containing preparations are used more often in the United Kingdom than they are in the United States. The side effects of irritation and staining can be reduced with short-contact therapy. Anthralin (Anthra-Derm, Lasan) is applied to lesions for 20 to 30 minutes, then washed

off. SYSTEMIC AGENTs-Systemic medications have produced significant improvement in some, but not all, patients with severe, extensive psoriasis. The retinoids

(eg, etretinate [Tegison]), methotrexate, and hydroxyurea (Hydrea) should be used only by those well versed in their potential side effects. When psoriatic plaques are thick but few and relatively small, use of intralesional triamcinolone acetonide, 5 to 10 mg/mL, helps flatten them. The most common undesired effects of this treatment are hypopigmentation and fat atrophy. Generally, an intralesional injection should not be given more often than once every 4 weeks. Still under study is acitretin (Soriatane), a metabolite of etretinate. This new retinoid offers the promise of efficacy with fewer side effects and less potential for teratogenicity. The immunosuppressive agent cyclosporine (Sandimmune) has also shown some promise in the treatment of psoriasis. In recent studies, both oral and intralesional forms have been shown to be effective in improving psoriasis. Until concerns about side effects and mutagenicity are resolved, however, cyclosporine will not be approved for this application. In patients who are infected with the human immunodeficiency virus (HIV) and have severe recalcitrant psoriasis, the

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Patients undergoing UV light therapy for psoriasis should be warned of and examined for resultant actinic damage, including carcinomas.

Figure 1. Plants that cause contact dermatitis. a. Poison ivy (left) and poison sumac (upper right). Brilliant red is typical of fall coloring. b. Complex flowers of Queen Anne's lace (wild carrot), a plant in the Umbelliferae family.

usual forms of treatment are not always effective. Some psoriatic HIV-positive patients have reportedly improved while undergoing zidovudine (Retrovir) treatment alone. Systemic and topical preparations of vitamin D and even fish oil are also under investigation for treatment of psoriasis. uv LIGHT-Not uncommonly, psoriatic lesions are widespread or are located in such areas as the palms and soles, where topical therapy alone may not be completely effective. In these circumstances, UV light may be more useful. In general, this form of treatment should be used only by a dermatologist formally trained

in phototherapeutic techniques. The combination of UVB and a topical coal tar preparation represents the modified Goeckerman regimen. When this regimen is combined with anthralin applied topically, it is referred to as the lngram regimen. A combination of UV light in the A range (UVA) and psoralen constitutes the PUVA regimen. Patients undergoing phototherapy should routinely be warned of and examined for resultant actinic damage, including carcinomas. The occurrence of genital carcinomas in men exposed to UV light has been reported in both the medical and the lay press. Thus, protection of

the genital area during treatments is important. Contact dermatitis The increase in outdoor activities during the warm seasons of the year heightens the problems with contact dermatitis and its attendant complications. SOURCFS OF ANTIGEN-The most common sources of contact dermatitis throughout the United States are the toxic plants in the Toxicodendron (formerly classified as Rhus) genus. These include poison ivy (T radicans). Depending on the area of the country, the particular species may vary. Moreover, in different plants in the genus, the active sensitizer

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Ragweed pollen has an oleoresin that occasionally produces the same contact dermatitis as that seen with poison ivy.

Figure 2. Typical lesion of contact dermatitis. Erythema and vesicles in linear pattem are produced by brushing against antigen. This appearance is perhaps the best clue to diagnosis.

represents a large number of related but different compounds. Almost all are oleoresins, lipidsoluble substances whose concentration varies among plants and whose potency varies among the different subsets of compounds. In the Toxicodendron genus, the number of identified oleoresins exceeds 40. Most of the Toxicodendron species are understory plants in the forest; some are vines, and some are small shrubs. Poison ivy and its relatives have a broad range of tolerance for soil and moisture conditions, and the plants often are spread · by wildlife. Most sensitive persons eventually learn to identifY the plant and avoid it. Some areas of the West Coast have very high concentrations of poison oak (T quercifolium); in the Mid-

west, large areas alongside roads and fence rows have similarly high concentrations of poison ivy, creating significant problems for people who work outdoors (eg, telephone line workers) in these areas. Poison sumac (T vernix) (figure 1a) also causes dermatitis on contact. The poisonous form can be confused with the many nonpoisonous sumacs found in much of the United States. The differences between the two are simple: Poison sumac has white berries and usually grows in moist lowlands, whereas nonpoisonous sumac has red berries and grows in dry uplands. Those who work or play outdoors are at risk for allergic reactions. In the fall, the burning of leaves can vaporize oleoresins, producing an airborne spread

that causes diffuse contact dermatitis. Other plants in the Toxicodendron genus include cashews, mangoes, and the Japanese lacquer tree. These urushiols are ubiquitous and pose a problem for sensitive persons who want to enjoy the outdoors when traveling outside the United States. Although the Toxicodendron genus is the prototype, there are a large number of other plants capable of causing contact dermatitis. The largest group is the Umbelliferae. This is a very large family of plants with complex daisylike flowers (figure 1b) that can reproducibly cause contact dermatitis in sensitive patients. The large number of species results in widespread potential for exposure of sensitive patients engaged in outdoor activities. Some plant pollens may also cause contact dermatitis. For example, ragweed pollen has an oleoresin that occasionally produces the same contact dermatitis as that seen with poison ivy. An additional related problem is plant-induced contact dermatitis resulting from changes in the antigen after exposure to sunlight (phytophotodermatitis). Cenain plants of the citrus, wild carrot, and wild parsley families are ea-

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Occasionally, plants serve as hosts to other organisms that produce contact or photocontact dermatitis.

pable of causing this problem. By themselves, the oleoresins do not cause significant dermatitis. However, after deposition of these oleoresins on the skin, exposure to UV light or sunlight results in the appearance of the linear array oflesions (figure 2) typical of contact dermatitis. The compounds here are related to psoralens, those photosensitizing chemicals used in PUVA treatment of psoriasis. Some sources of the antigen are unusual. Pets and other fomites (eg, clothing) must be considered. Occasionally, plants serve as hosts to other organisms that produce contact or photocontact dermatitis. The best example of this is the pink celery rot that has caused recurring epidemics of photocontact dermatitis in agricultural workers who harvest celery. They get psoralen-containing celery rot on their hands, and subsequent exposure to sunlight or UV light results in sunburn or linear blisters. The treatment of contact or photocontact dermatitis from these plants is not different from that of Toxicodendron dermatitis. PRESENTATION-The response in exposed persons varies according to the degree of sensitivity, amount of oleoresin, and extent

Table 1. Corticosteroids used to treat contact dermatitis In mild cases Mid-strength topical corticosteroids Triamcinolone acetonide (various) Diflorasone diacetate (Maxiflor) Fluticasone propionate (Cutivate) Mometasone furcate (Eiocon) Menthol and camphor lotions (eg, Sarna) Pramoxine HCI (PrameGel)

In severe cases Systemic corticosteroids Prednisone, 1 mg/kg, usually tapering over 10 to 18 days Potent topical corticosteroids Augmented betamethasone dipropionate (Diprolene) Clobetasol propionate (Temovate) Diflorasone diacetate (Fiorone) Halobetasol propionate (Uitravate)

of contact. A history of recent outdoor activity and the presence of the classic linear array oflesions are usually sufficient to establish the diagnosis. Confusion about diagnosis occurs only occasionally; such cases often involve patients who have never had problems with contact dermatitis before. TIIERAPY-During the initial visit, the patient should be told the cause of the problem and taught to identify and avoid the source of the antigen in the fu-

ture. The patient should also be cautioned to remove the antigen as soon as possible after exposure; warm, soapy water is all that is necessary. The aggressiveness of therapy is generally proponional to the severity of the reaction. Selecting the appropriate level of therapy depends on the results of a careful, complete examination. The patient should be advised that relief of symptoms is not instantaneous but should occur in the next 48 to 96 hours.

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Systemic corticosteroid therapy is generally reserved for patients with a history of severe, widespread contact dermatitis or those with involvement of more than 30% of the body.

TOPICAL AGENTs-Mild cases of contact dermatitis are usually treated with topical corticosteroids (table 1). Newer, potent corticosteroids control both the symptoms and the spread of dermatitis. It is rarely necessary to use antipruritics. Adjunctive use of menthol and camphor lotions, cool soaks, and wet-to-dry soaks may be helpful in controlling pruritus. SYSTEMIC AGENTS-Use of systemic corticosteroids is generally reserved for patients who have a history of severe, widespread reactions or those in whom more than 30o/o of the body is involved. Patients with involvement of the hands, face, or genitals also are candidates for aggressive systemic corticosteroid therapy. Prednisone is usually the preferred agent, and the dose is 1 to 2 mg/kg. The higher dose is used in patients with a higher degree of sensitivity. Patients who are at risk for complications of fluid retention due to the mineralocorticoid effects of prednisone may benefit from the substitution of dexamethasone (Decadron, Dexone, Hexadrol), usually in a dose of 0.75 mg/kg. We find this agent to be particularly effective in older patients with cardiac problems and patients taking diuret-

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ics. The dosage we use is considerably more than that provided in most commercially available, prepackaged, dosage-tapering products. In our experience, the most common problem in patients unresponsive to therapy is inadequate dosage. PROPHYLAXIS-On initial examination, patients with severe, widespread contact dermatitis should be assessed for potential or existing secondary infection. In the summer in warm climates, infections secondary to widespread Toxicodendron dermatitis are the rule rather than the exception, and under these circumstances, antibiotic therapy is often initiated prophylactically. The antibiotic of choice varies from region to region, depending on the indigenous pathogens and their sensitivity profiles. The usual dosage-by-weight standard applies. Until recently, erythromycin perhaps was the favored antibiotic, but increasing staphylococcal resistance to it is making it a less desirable choice. Exquisitely sensitive patients with recurring episodes of contact dermatitis should also be advised of certain prophylactic measures. Hyposensitization has had a variable record; indeed, intramuscular poison ivy shots have been the biggest cause of this variability in response. Even

the oral hyposensitization rate is not consistent or predictable, since there is no direct assay to determine potency and the batch-to-batch sources of the antigen vary in concentration. Nevertheless, the oral approach remains the only approach and in the best of all possible circumstances is largely effective. Particularly useful for sensitive patients who have occupational exposure is the use of barrier creams.

Common warts Approaches to the treatment of common warts have proliferated in the last few years. At the same time, understanding of the causative viruses has expanded. PRFSEN11\TION-Newer techniques have allowed researchers to separate and define many new human papillomavirus (HPV) types; their number grows each year. Warts caused by certain HPV types are potentially premalignant; otherwise, their significance for practitioners is not clear at present. Technology to identifY HPV types is evolving and should be available in the next few years. In patients with persistent warts, determination of the type is important; more aggressive therapy is indicated if the HPV type is one with increased malignant potential.

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Significant discomfort occurs immediately after cryotherapy for common warts; the pain after vesicant application is delayed, if it occurs at all.

1HERAPY-Simple nonvenereal warts may respond to a variety of over-the-counter preparations. Many patients try one or more of these preparations to no avail before seeking medical attention; as a result, they are likely to require more aggressive therapy on the first medical visit. Some preparations available for treating nonvenereal warts are listed in table 2. CRYOTHERAPY AND CHEMICAL

AGENTS-Almost all treatments for warts are destructive. Usually, the most useful initial approach is cryosurgery with liquid nitrogen, freezing the wart and about 1 mm of surrounding tissue to be certain of in-depth destruction of the wart. In our estimation, it is better to err on the conservative side and re-treat a patient than run the risk of creating a severe, deep bulla with the potential for a painful scar. If one or more cryosurgery treatments fail to eradicate the wart, chemical treatment with cantharidin (Cantharone) or one of its keratolytic combinations (Cantharone Plus, Verrusol) often is the next step. The primary active ingredient in all these substances is vesicant material from blister beetles. The keratolytics are combined with podophyllin, which lends additional help in destroying the wart.

Cantharidin should be applied to the wart, allowed to dry thoroughly for 5 to 10 minutes, and then kept from migrating by putting moleskin over the wart and plain adhesive tape over that. This nearly always results in a blister with the wart in the blister roo£ The blister is then protected and allowed to dry, desquamating the remains of the wart. Multiple treatments are sometimes necessary, and occasionally this causes considerable discomfort. The primary difference between cryotherapy and vesicant therapy is that significant discomfort occurs immediately with cryotherapy, whereas the pain after vesicant application is delayed, if it occurs at all. In our estimation, the use of vesicants is perhaps the single most valuable approach to treatment of warts that have been refractory to virtually all other methods. The technique must be used very carefully and the blister protected to get the best result. For multiple (mosaic) warts, a systematic, stepwise approach to eradication is necessary, but this may be time-consuming for both physician and patient. With both cryotherapy and vesicant therapy, rosetting (ie, development of warts around the edge of the blister) is a recognized risk that usu-

Table 2. Over-the-counter and prescription preparations for wart therapy Over-the-counter Mediplast (for plantar use)

Prescription Duofilm Occlusal Occlusal-HP Trans-Ver-Sal Trans-Piantar (for plantar use) Cantharidin alone or in combination (Cantharone, Cantharone Plus, Verrusol) Podofilox (Condylox) Viranol (gel)

ally cannot be avoided. After the initial visit, the patient should apply a vesicant to the area around the warts as well as to the warts themselves, since this sometimes diminishes recurrence in the periphery. We also have found that application ofliquid tretinoin 0.05% is a useful method for treating multiple recalcitrant warts. Use of this liquid on tissue surround-

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Unusual-appearing lesions of condyloma acuminatum seem to have increased malignant potential.

ing wart sites seems to diminish the potential for new or recurring wans. SURGERY-Surgical therapy is another approach to consider. It involves anesthetizing the area and using a dermal curet to bluntly dissect the wart. This takes considerable experience, but once the skill is acquired, the extent of the wart can be easily delineated for complete removal. However, as with any surgical technique, caution is imponant because of the potential for scarring. Scars on the hands or feet can be very painful, and we have seen cases in which surgical treatment resulted in a painful scar that contained recurrent warts. Nevertheless, for very large warts, this procedure performed by an experienced surgeon may be the most expeditious way to decrease wart volume and effect clearing. TRANSDERMAL PATCHES-The newest approach to treatment of nonvenereal warts is transdermal delivery of salicylates and other agents to destroy the wart. Transdermal patches (Trans-Ver-Sal, Trans-Plantar) have proved to be more effective than older overthe-counter preparations against problem warts. If this approach fails, other methods, including surgery, may be necessary.

IMMUNOTHERAPY-Occasionally, all the aforementioned approaches are not sufficient. Under these circumstances, the next generation of therapy is appropriate; this includes immunotherapy with T-cell stimulants to enhance the host's ability to reject the wart. This approach is still experimental. Various biologic molecules, including interferon, are now being studied for effectiveness against warts. Immunotherapy remains the last resort and is used primarily by dermatologists. We have found it to be most useful in very difficult cases of recurrent or recalcitrant warts. Venereal warts The problem of malignant potential seems greater for condyloma acuminatum than for common nonvenereal warts. It has been given increased attention in the literature and perhaps has been one of the major reasons for the enhanced study and interest in the various viral subtypes. PRESENTATION-Unusualappearing condylomas seem to have increased malignant potential. The epidemiology of condyloma acuminatum perhaps will be better understood as typing of HPVs becomes easier and more

commonplace, allowing better identification of sources of transmiSSiOn.

lHERAPY-Traditionally, condyloma acuminatum has been treated with several podophyllin resin preparations (eg, Podofin). These agents have not been considered appropriate for home therapy because of the potential for side effects; toxicity has occasionally been reported with the use of a large amount of podophyllin. We believe that treatment with podophyllin is still the simplest and best firstline approach. A purified podophyllin, podofilox (Condylox), has a better safety profile than the podophyllin resins and thus has been approved for home use. This agent may be helpful to busy practitioners. However, patients often complain of irritation and burning. Nonetheless, for patients who cannot make multiple visits for recurring therapy, podofilox may be a useful alternative. We routinely caution patients about its side effects. In patients who have large numbers of small, papular venereal warts, identification and treatment may be prolonged. Under these circumstances, podofilox may be useful. In patients who have very small, flat, papular

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lesions, some of which do fit the premalignant category, this home treatment may achieve complete eradication. We have also obtained good results with liquid tretinoin 0.05% in such patients.

Summary The therapeutic approaches to the five common skin problems described range from standard topical and systemic agents to newly introduced alternative medications and techniques. In acne, the type of lesion found on physical examination determines the severity of the disease and its subsequent treatment. When necessary, appropriate precautions must be taken before and during therapy. Fortunately, with the drugs available today; only the most extreme cases of acne should progress to the stage where physical and/or psychological scarring occurs. The number of therapeutic approaches to psoriasis, from steroids to UV light, pays testament to the difficulty in treating this cyclic disease. Until an effective and safe medication is developed, research is sure to continue.

Sources of the antigen causing contact dermatitis are sometimes unusual, but the lesions have a characteristic appearance. Several topical and systemic agents are available. Patient education and prophylactic measures play an important role. Therapies for both venereal and nonvenereal warts are proliferating. The evolving understanding of viral oncogenesis in both types of warts promises that this will be an area of continued intense research in the next few years. FUIII

-@

Earn credit on this article. See CME Quiz.

Address for correspondence: Larry E. Millikan, MD, 1430 Tulane Ave, New Orleans, LA 70112.

References 1. Nazzaro-Porro M. Azelaic acid. J Am Acad Dermaroll987;17(6):1033-41 2. Schachner L, Pestano A, Kitties C. A clinical trial comparing the safery and efficacy of a ropical erythromycin-zinc formulation with a ropical clindamycin formulation. J Am Acad Dermarol 1990;22(3):489-95 3. Hughes BR, Norris JFB, Cunliffe WJ. A double-blind evaluation of ropical isotretinoin, benwyl perioxide, and placebo in patients with acne. Br J Dermatol 1989;12I(Suppl34):42

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An update on common skin diseases. Acne, psoriasis, contact dermatitis, and warts.

The therapeutic approaches to the five common skin problems described range from standard topical and systemic agents to newly introduced alternative ...
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